The lab is interested in understanding molecular and cellular mechanisms underlying synapse formation and synaptic plasticity, and in the long term elucidating synaptic mechanisms underlying neuronal circuit function in animal behavior. We believe that these studies will provide fundamental insights into neural underpinnings for learning and memory, and will identify synaptic and neural circuit malfunctions that are involved in many neurological and mental disorders, such as epilepsy, Alzheimer's disease, depression and autism. Specifically, during the 2018 fiscal year, we have made following progress: For research Aim 1: we have successfully determined the role of FRRS1L, a transmembrane protein that binds to AMPARs, in the regulation of excitatory synaptic strength. Currently one manuscript for this work has been published in Frontiers in Molecular Neuroscience. For research Aim 2, we have identified a novel protein interacting with GABA-A receptors. Currently we have made substantial progress in determining the function of this protein in the regulation of GABAergic synaptic transmission. We plan to submit a manuscript describing these data by the end of 2018. For research Aim 3: we have established a general molecular framework essential for GABAergic synapse development in hippocampus. Currently, a manuscript for this work has been published in Neuron. In addition, we have made important progress in determining the molecular mechanisms underlying GABAergic synapse development, including how trans-synaptic interactions regulate GABAergic synapse development and how NMDARs mediate signaling for GABAergic synaptogenesis. Finally, during the 2018 fiscal year, we have collaborated with Dr. Katherine Roche group at NINDS, NIH to study the function of Neuroligin1 in the regulation of excitatory synaptic transmission. In addition, we have collaborated with Dr. Chris McBain lab at NICHD, NIH to study the role of the interaction between Neuroligin2 and Slitrk3 in the regulation of GABAergic synapses, which led to a publication in Neuron. We have also collaborated with Dr. Thomas Hnasko lab at UCSD to study the role of vGluT2 in the selective vulnerability of dopamine neurons in Parkinsons diseases, which led to a publication in Journal of Clinical Investigation. Furthermore, we have collaborated with Dr. Juan Song at UNC Chapel Hill to study the role of glutamate receptors in adult neurogenesis in hippocampus, which led to a publication in Neuron.